Erythrocyte Sodium Transport, Intraplatelet pH, and Calcium Concentration in Salt-Sensitive Hypertension

Lluch, M.; Sierra, Alejandro de la; Poch, Esteban; Coca, António; Aguilera, Mònica; Compte, Montserrat; Urbano-Márquez, Á

doi:10.1161/01.hyp.27.4.919

Cited by 21 publications

(5 citation statements)

References 33 publications

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“…Although salt sensitivity is a well established phenomena in experimental and human hypertension, the pathophysiologic mechanisms remain unclear. It has been suggested that abnormalities in the renin angiotensin aldosterone system 20 21) , the sympathetic nervous system 22) , renal transmembrane sodium transport 23) , the kallikrein-kinin system, the nitric oxide (NO) system, eicosanoids, and the vascular endothelium 24 25) are all involved in the pathogenesis of salt sensitive hypertension. In the evolutionary aspects, human kidneys are well-equipped with a salt retaining function and have less efficient salt excretory functions when challenged with large amounts of salt loads.…”

Section: Introductionmentioning

confidence: 99%

Salt Sensitivity and Hypertension: A Paradigm Shift from Kidney Malfunction to Vascular Endothelial Dysfunction

Choi

Park

2015

Electrolyte Blood Press

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Hypertension is a complex trait determined by both genetic and environmental factors and is a major public health problem due to its high prevalence and concomitant increase in the risk for cardiovascular disease. With the recent large increase of dietary salt intake in most developed countries, the prevalence of hypertension increases tremendously which is about 30% of the world population. There is substantial evidence that suggests some people can effectively excrete high dietary salt intake without an increase in arterial BP, and another people cannot excrete effectively without an increase in arterial BP. Salt sensitivity of BP refers to the BP responses for changes in dietary salt intake to produce meaningful BP increases or decreases. The underlying mechanisms that promote salt sensitivity are complex and range from genetic to environmental influences. The phenotype of salt sensitivity is therefore heterogeneous with multiple mechanisms that potentially link high salt intake to increases in blood pressure. Moreover, excess salt intake has functional and pathological effects on the vasculature that are independent of blood pressure. Epidemiologic data demonstrate the role of high dietary salt intake in mediating cardiovascular and renal morbidity and mortality. Almost five decades ago, Guyton and Coleman proposed that whenever arterial pressure is elevated, pressure natriuresis enhances the excretion of sodium and water until blood volume is reduced sufficiently to return arterial pressure to control values. According to this hypothesis, hypertension can develop only when something impairs the excretory ability of sodium in the kidney. However, recent studies suggest that nonosmotic salt accumulation in the skin interstitium and the endothelial dysfunction which might be caused by the deterioration of vascular endothelial glycocalyx layer (EGL) and the epithelial sodium channel on the endothelial luminal surface (EnNaC) also play an important role in nonosmotic storage of salt. These new concepts emphasize that sodium homeostasis and salt sensitivity seem to be related not only to the kidney malfunction but also to the endothelial dysfunction. Further investigations will be needed to assess the extent to which changes in the sodium buffering capacity of the skin interstitium and develop the treatment strategy for modulating the endothelial dysfunction.

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Section: Introductionmentioning

confidence: 99%

Salt Sensitivity and Hypertension: A Paradigm Shift from Kidney Malfunction to Vascular Endothelial Dysfunction

Choi

Park

2015

Electrolyte Blood Press

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“…[23][24][25] Compared with SSBP, these subjects had decreased left ventricular mass and septal and posterior wall thickness with no difference in internal diastolic diameter, increased HDL (high-density lipoprotein), decreased total cholesterol/HDL and decreased red cell Na/K pump, cotransport and counter transport activity. 23,25,26 Neither arterial pressure nor sympathetic activity is dependent on salt intake in individuals without versus those with SSBP. 27 Fenofibrate has no effect on BP, heart rate, or renal vasoconstriction in subjects without versus with SSBP.…”

Section: Discussionmentioning

confidence: 99%

Role of Raptor Gene Variants in Hypertension: Influence on Blood Pressure Independent of Salt Intake in White Population

Aljaibeji,

Heydarpour,

Stanton

et al. 2024

Hypertension

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BACKGROUND: The mTOR (mechanistic target of rapamycin) is an essential regulator of fundamental biological processes. mTOR forms 2 distinct complexes, mTORC1 (mTOR complex 1) when it binds with RAPTOR (Regulatory-associated Protein of mTOR) and mTORC2 (mTOR complex 2) when it associates with RICTOR (Rapamycin-insesitive companion of mTOR). Due to the previous link between the mTOR pathway, aldosterone, and blood pressure (BP), we anticipated that variants in the mTOR complex might be associated with salt-sensitive BP. METHODS: BP and other parameters were assessed after a one-week liberal Na + (200 mmol/d) and a one-week restricted Na + (10 mmol/d) diet in 608 White subjects from the Hypertensive Pathotype cohort, single-nucleotide variants in MTOR , RPTOR , and RICTOR genes were obtained for candidate genes analyses. RESULTS: The analysis revealed a significant association between a single nucleotide variants within the RPTOR gene and BP. Individuals carrying the RPTOR rs9901846 homozygous risk allele (AA) and heterozygous risk allele (GA) exhibited a 5 mm Hg increase in systolic BP on a liberal diet compared with nonrisk allele individuals (GG), but only in women. This single nucleotide variants effect was more pronounced on the restricted diet and present in both sexes, with AA carriers having a 9 mm Hg increase and GA carriers having a 5 mm Hg increase in systolic BP compared with GG. Interestingly, there were no significant associations between MTOR or RICTOR gene variants and BP. CONCLUSIONS: The RPTOR gene variation is associated with elevated BP in White participants, regardless of salt intake, specifically in females.

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“…Hence, only a defect in renal natriuretic system would explain a salt-induced elevation in BP. Indeed, extensive research has found various alterations in renal Na + channels (16 –19), the renin-angiotensin system (20 –22), and the sympathetic system (23 –26) in salt-sensitive hypertension. Nevertheless, the precise pathogenesis of salt sensitivity remains controversial.…”

Section: Pathophysiology Of Salt-sensitive Hypertensionmentioning

confidence: 99%

Dendritic Cell Epithelial Sodium Channel in Inflammation, Salt-Sensitive Hypertension, and Kidney Damage

Ertuğlu

Kirabo

2022

Kidney360

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Salt-sensitive hypertension is a major risk factor for cardiovascular morbidity and mortality. The pathophysiologic mechanisms leading to different individual BP responses to changes in dietary salt remain elusive. Research in the last two decades revealed that the immune system plays a critical role in the development of hypertension and related end organ damage. Moreover, sodium accumulates nonosmotically in human tissue, including the skin and muscle, shifting the dogma on body sodium balance and its regulation. Emerging evidence suggests that high concentrations of extracellular sodium can directly trigger an inflammatory response in antigen-presenting cells (APCs), leading to hypertension and vascular and renal injury. Importantly, sodium entry into APCs is mediated by the epithelial sodium channel (ENaC). Although the role of the ENaC in renal regulation of sodium excretion and BP is well established, these new findings imply that the ENaC may also exert BP modulatory effects in extrarenal tissue through an immune-dependent pathway. In this review, we discuss the recent advances in our understanding of the pathophysiology of salt-sensitive hypertension with a particular focus on the roles of APCs and the extrarenal ENaC.

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Erythrocyte Sodium Transport, Intraplatelet pH, and Calcium Concentration in Salt-Sensitive Hypertension

Cited by 21 publications

References 33 publications

Salt Sensitivity and Hypertension: A Paradigm Shift from Kidney Malfunction to Vascular Endothelial Dysfunction

Salt Sensitivity and Hypertension: A Paradigm Shift from Kidney Malfunction to Vascular Endothelial Dysfunction

Role of Raptor Gene Variants in Hypertension: Influence on Blood Pressure Independent of Salt Intake in White Population

Dendritic Cell Epithelial Sodium Channel in Inflammation, Salt-Sensitive Hypertension, and Kidney Damage

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